Chronic back pain is an epidemic. Nerve impingement is not seen by CT or MRI in about 85% of back pain patients [Deyo R A, Weinstein J N: Low back pain, N Eng J Med, 344(5) February 363-370, 2001. Boswell M V, et. al.: Interventional Techniques: Evidence-based practice guidelines in the management of chronic spinal pain, Pain Physician, 10:7-111, ISSN 1533-3159, 2007]. In fact, lumbar disc prolapse, protrusion, or extrusion accounts for less than 5% of all low back problems, but are the most common causes of nerve root pain and surgical interventions (Manchikanti L, Derby R, Benyamin R M, Helm S, Hirsch J A: A systematic review of mechanical lumbar disc decompression with nucleoplasty, Pain Physician; 12:561-572 ISSN 1533-3159, 2009). The cause of chronic back pain in most patients has been puzzling to both physicians and patients. Disc contains no blood vessels. Oxygen, nutrients and pH buffer in fluid of body circulation are diffused from capillaries at endplates into the thick and avascular disc. However, calcified layers begin to fortify the cartilaginous endplates as early as age 16, blocking capillaries and reducing diffusion depths of oxygen, nutrients and pH buffer into the disc. Shallow diffusion zones of oxygen, nutrients and neutral pH do not extend into mid-layer of the disc. Hypoxia triggers formation of lactic acid and inflammation in mid-layer of the disc, resulting in acidic pH 5.5-6.5. Starvation triggers enzymatic degradation of proteoglycans in disc matrix to feed cells and form cavities and fissure in the mid-layer. Lactic acid and inflammatory cytokines leak from fissure to inflame outer annulus, causing chronic discogenic pain. Enzymatic degradation of disc matrix flattens the disc, shifting the compressive load from the thinning disc to facet joints, causing facet strain and pain. Both lactic acid burn and strain of the facet joints are not visible under CT or MRI.
Urinary incontinence is common among women after multiple pregnancies. Weight of the baby partially rests on the bladder, flattening and widening the bladder neck and urethral lumen. The sphincteric action of the urethral smooth muscle cannot contract far enough to close the widened lumen for coaptation of urethral mucosa, resulting in urinary incontinence.